Partly reversible central auditory dysfunction induced by cerebral vasospasm after subarachnoid hemorrhage

2013 ◽  
Vol 119 (5) ◽  
pp. 1125-1128 ◽  
Author(s):  
Ester Ponzetto ◽  
Marco Vinetti ◽  
Cécile Grandin ◽  
Thierry Duprez ◽  
Vincent van Pesch ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Auditory Evoked Potentials ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rare Complication ◽  
Brain Mri ◽  
Temporal Cortex ◽  
Intraarterial Infusion ◽  
Auditory Dysfunction ◽  
The Right

The authors describe a rare case of central auditory dysfunction induced by cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). A 55-year-old woman who was admitted after aneurysmal SAH developed cerebral vasospasm on Day 3 affecting mainly the right middle cerebral artery (MCA) and partly the left MCA. The vasospasm became refractory to conventional therapy and was ultimately improved by intraarterial infusion of nimodipine in the right MCA and angioplasty. Severe auditory dysfunction was apparent from Day 10 as the patient was not reactive to speech or environmental sounds. Brain MRI on Day 17 demonstrated infarcted areas mainly in the right hippocampus, medial occipital lobe, and thalamus. The patient underwent further examination using audiometry, speech testing, auditory evoked potentials, functional MRI, and cerebral PET. The initial diagnosis was extended nonverbal agnosia and total pure word deafness. The central auditory dysfunction improved over 6 months, with persisting hyperacusis, tinnitus, and amusia. Central auditory dysfunction is a rare complication after SAH. While cortical deafness may be associated with bilateral lesions of the temporal cortex, partly reversible central auditory dysfunction was observed in this patient after prominently unilateral right temporal lesions. The role of the interthalamic connections can be discussed, as well as the possibility that a less severe vasospasm on the left MCA could have transiently impaired the left thalamocortical auditory pathways.

scholarly journals Cerebral Vasospasm with Ischemia following a Spontaneous Spinal Subarachnoid Hemorrhage

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Sophia F. Shakur ◽  
Hamad I. Farhat
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Brain Mri ◽  
International Normalized Ratio ◽  
Unique Case ◽  
First Case ◽  
Spinal Subarachnoid Hemorrhage ◽  
Spine Mri

Cerebral vasospasm is a well-known consequence of aneurysmal subarachnoid hemorrhage (SAH) triggered by blood breakdown products. Here, we present the first case of cerebral vasospasm with ischemia following a spontaneous spinal SAH. A 67-year-old woman, who was on Coumadin for atrial fibrillation, presented with chest pain radiating to the back accompanied by headache and leg paresthesias. The international normalized ratio (INR) was 4.5. Ten hours after presentation, she developed loss of movement in both legs and lack of sensation below the umbilicus. Spine MRI showed intradural hemorrhage. Her coagulopathy was reversed, and she underwent T2 to T12 laminectomies. A large subarachnoid hematoma was evacuated. Given her complaint of headache preoperatively and the intraoperative finding of spinal SAH, a head CT was done postoperatively that displayed SAH in peripheral sulci. On postoperative day 5, she became obtunded. Brain MRI demonstrated focal restricted diffusion in the left frontoparietal area. Formal angiography revealed vasospasm in anterior cerebral arteries bilaterally and right middle cerebral artery. Vasospasm was treated, and she returned to baseline within 48 hours. Spontaneous spinal SAH can result in the same sequelae typically associated with aneurysmal SAH, and the clinician must have a degree of suspicion in such patients. The pathophysiological mechanisms underlying cerebral vasospasm may explain this unique case.

Abstract 3499: Novel Nitric Oxide-Containing Echogenic Liposome for the Treatment of Vasospasm Following Subarachnoid Hemorrhage

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
George L Britton ◽  
Tao Peng ◽  
Jaroslaw Aronowski ◽  
David D McPherson ◽  
Shao-Ling Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Femoral Vein ◽  
High Morbidity ◽  
Sprague Dawley ◽  
Treatment Groups ◽  
Echogenic Liposomes ◽  
The Right

Background: Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of high morbidity and mortality. The reduced availability of nitric oxide (NO) in blood and cerebrospinal fluid (CSF) is suggested an important mechanism underlying cerebral vasospasm, a complication of SAH. NO or NO donors are known to have potent effects on cerebral vascular relaxation. We have developed NO-containing echogenic liposomes (NO-ELIP) for NO delivery to assess the role of NO in SAH-induced vasospasm. We hypothesized that NO-ELIP can produce vasodilation and provide an effective therapeutic approach to treat vasospasm following SAH. Methods: NO-ELIP was created by a freeze-under-pressure method. Male Sprague- Dawley rats (n=9) underwent SAH by puncturing the right middle cerebral artery with a sharp tip nylon monofilament. In the treatment groups, NO-ELIP were administered through the right femoral vein at 24 hours after SAH onset. The brain tissue was obtained for H&E staining at 30 min after NO-ELIP administration. Measurement of the posterior communicating artery was performed to evaluate the effects of NO-ELIP treatment on vasospasm following SAH. Results: After SAH, the normalized lumenal and wall thickness areas decreased from 1.02 ± 0.08 to 0.40 ± 0.15 (p<0.001). NO-ELIP inhibited SAH-induced vasospasm by 67% (normalized area decreased to 0.82 ± 0.10 (p=0.004). Conclusion: This study demonstrates that NO-ELIP have the potential to deliver NO for therapeutic treatment of vasospasm. Enhancing the release of NO from circulating NO-ELIP by combining ultrasound exposure over the carotid artery may further provide an improved treatment strategy. This suggests that targeted therapeutic gas can be delivered to the cerebral circulation for the treatment of vasospasm following SAH

Reversible cortical auditory dysfunction caused by cerebral vasospasm after ruptured aneurysmal subarachnoid hemorrhage and evaluated by perfusion magnetic resonance imaging

2007 ◽  
Vol 107 (1) ◽  
pp. 161-164 ◽  
Author(s):  
Sadaharu Tabuchi ◽  
Mitsutoshi Kadowaki ◽  
Takashi Watanabe
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Magnetic Resonance ◽  
Mr Imaging ◽  
Cerebral Vasospasm ◽  
Mean Transit Time ◽  
Auditory Brainstem Responses ◽  
Perfusion Magnetic Resonance Imaging ◽  
Mr Images ◽  
Auditory Dysfunction ◽  
The Right

✓ A 52-year-old woman developed subarachnoid hemorrhage (SAH) caused by a ruptured right internal carotid artery (ICA) aneurysm. Because of the aneurysm configuration, the authors decided to delay surgery and instead undertook serial imaging studies of the aneurysm. The patient remained alert but developed acute bilateral deafness on Day 7. Audiological examination and auditory brainstem responses suggested that the hearing disturbance was cortical in origin. Three-dimensional computed tomography (CT) angiography showed severe vasospasm in the right middle cerebral artery (MCA) and moderate vasospasm in the left ICA and MCA. Three-tesla magnetic resonance (MR) imaging was performed 2 days after the onset of symptoms. Diffusion-weighted and T2-weighted MR images showed an acute infarction in the right insular cortex caused by vasospasm. Perfusion-weighted MR imaging, particularly mean transit time mapping, revealed hypoperfusion in both temporal lobes including the auditory cortex and right auditory radiation. The vasospasm was treated with induction of mild hypertension and hypervolemia. Follow-up MR images, 3D CT angiograms, and audiometry performed 2 weeks after the first examination showed recovery of vasospasm and resolution of perfusion abnormality and hearing disturbance. On Day 26, the aneurysm was successfully occluded with clips and the patient was discharged with no deficits. To the authors' knowledge, this is the first reported case of reversible cortical auditory dysfunction purely due to bilateral cerebral vasospasm detected using perfusion MR imaging after SAH.

Effect of Cilostazol on Cerebral Vasospasm and Outcome in Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized, Double-Blind, Placebo-Controlled Trial

2016 ◽  
Vol 42 (1-2) ◽  
pp. 97-105 ◽  
Author(s):  
Naoya Matsuda ◽  
Masato Naraoka ◽  
Hiroki Ohkuma ◽  
Norihito Shimamura ◽  
Katsuhiro Ito ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Independent Factor ◽  
Double Blind ◽  
End Points ◽  
Double Blind Placebo ◽  
Poor Outcome

Background: Several clinical studies have indicated the efficacy of cilostazol, a selective inhibitor of phosphodiesterase 3, in preventing cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). They were not double-blinded trial resulting in disunited results on assessment of end points among the studies. The randomized, double-blind, placebo-controlled study was performed to assess the effectiveness of cilostazol on cerebral vasospasm. Methods: Patients with aneurysmal SAH admitted within 24 h after the ictus who met the following criteria were enrolled in this study: SAH on CT scan was diffuse thick, diffuse thin, or local thick, Hunt and Hess score was less than 4, administration of cilostazol or placebo could be started within 48 h of SAH. Patients were randomly allocated to placebo or cilostazol after repair of a ruptured saccular aneurysm by aneurysmal neck clipping or endovascular coiling, and the administration of cilostazol or placebo was continued up to 14 days after initiation of treatment. The primary end point was the occurrence of symptomatic vasospasm (sVS), and secondary end points were angiographic vasospasm (aVS) evaluated on digital subtraction angiography, vasospasm-related new cerebral infarction evaluated on CT scan or MRI, and clinical outcome at 3 months of SAH as assessed by Glasgow Outcome Scale, in which poor outcome was defined as severe disability, vegetative state, and death. All end points were evaluated with blinded assessment. Results: One hundred forty eight patients were randomly allocated to the cilostazol group (n = 74) or the control group (n = 74). The occurrence of sVS was significantly lower in the cilostazol group than in the control group (10.8 vs. 24.3%, p = 0.031), and multiple logistic analysis showed that cilostazol use was an independent factor reducing sVS (OR 0.293, 95% CI 0.099-0.568, p = 0.027). The incidence of aVS and vasospasm-related cerebral infarction were not significantly different between the groups. Poor outcome was significantly lower in the cilostazol group than in the control group (5.4 vs. 17.6%, p = 0.011), and multiple logistic analyses demonstrated that cilostazol use was an independent factor that reduced the incidence of poor outcome (OR 0.221, 95% CI 0.054-0.903, p = 0.035). Severe adverse events due to cilostazol administration did not occur during the study period. Conclusions: Cilostazol administration is effective in preventing sVS and improving outcomes without severe adverse events. A larger-scale study including more cases was necessary to confirm this efficacy of cilostazol.

scholarly journals Risk factors for cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 598-604
Author(s):  
Valentina Opancina ◽  
Snezana Lukic ◽  
Slobodan Jankovic ◽  
Radisa Vojinovic ◽  
Milan Mijailovic
Keyword(s):  
Risk Factors ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Medical Center ◽  
White Blood Cells ◽  
Cerebral Aneurysms ◽  
International Normalized Ratio ◽  
Cross Sectional Study ◽  
Cross Sectional

AbstractIntroductionAneurysmal subarachnoid hemorrhage is a type of spontaneous hemorrhagic stroke, which is caused by a ruptured cerebral aneurysm. Cerebral vasospasm (CVS) is the most grievous complication of subarachnoid hemorrhage (SAH). The aim of this study was to examine the risk factors that influence the onset of CVS that develops after endovascular coil embolization of a ruptured aneurysm.Materials and methodsThe study was designed as a cross-sectional study. The patients included in the study were 18 or more years of age, admitted within a period of 24 h of symptom onset, diagnosed and treated at a university medical center in Serbia during a 5-year period.ResultsOur study showed that the maximum recorded international normalized ratio (INR) values in patients who were not receiving anticoagulant therapy and the maximum recorded white blood cells (WBCs) were strongly associated with cerebrovascular spasm, increasing its chances 4.4 and 8.4 times with an increase of each integer of the INR value and 1,000 WBCs, respectively.ConclusionsSAH after the rupture of cerebral aneurysms creates an endocranial inflammatory state whose intensity is probably directly related to the occurrence of vasospasm and its adverse consequences.

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